Biomedical subjects
Publications and source records attributed to V Puri.
This case report describes a patient in whom a descending aortic aneurysm ruptured into the left lung, producing hemoptysis. With transesophageal echocardiography, we were able to define the site and extent of the aneurysm, as well as the two sites of rupture into lung tissue.
We present the case of a patient with a single papillary muscle that is supporting both orifices of a stenotic double orifice mitral valve. With the use of both transthoracic and transesophageal echocardiography, we were able to prospectively define this entity, which was confirmed at surgery.
This case report describes a patient in whom a left internal carotid (LIC) artery stent was detected using a transpharyngeal approach during a transesophageal echocardiographic (TEE) study. Using pulsed-Doppler interrogation, flow through and beyond the stent was characterized and restenosis was ruled out.
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A 53 years old male, a known case of ankylosing spondylitis having recurrent attacks of hypoglycaemia, developed symmetrical distal sensorimotor neuropathy. The neuropathy was axonal with secondary demyelination. Evidence of vasculopathy was also noted on histopathology of the nerve. Serum C-peptide level was low, a feature reported with autoimmune hypoglycaemia with antireceptor antibodies. The patient showed spontaneous recovery.
BACKGROUND & OBJECTIVES: A sizeable number of epilepsy patients remain uncontrolled with carbamazepine (CBZ) monotherapy. While the therapeutic plasma concentration range of CBZ is only vaguely defined, pharmacokinetic differences in the disposition of CBZ among subjects could be responsible for the inadequate control of seizures in some. This study was aimed at associating serum CBZ levels with seizure control and elucidating any pharmacokinetic differences between patients with controlled and uncontrolled epilepsy. METHODS: The study was conducted in 16 controlled and 15 uncontrolled adult epileptic patients receiving CBZ monotherapy for the previous 3 or more months, without any dosage change. Blood samples were drawn from the patients before and 0.5, 1, 2, 3, 4, 8, 12 and 24 h after ingestion of their total daily dose of CBZ. Serum CBZ levels were measured by HPLC and the pharmacokinetic parameters were calculated. RESULTS: The uncontrolled epileptic patients were receiving a higher daily dose of CBZ (difference not significant). The trough and peak serum CBZ levels were relatively higher in the uncontrolled group, and at no time point were the drug levels lower in these patients compared to the controlled group. The absorption kinetics, volume of distribution and plasma half life of CBZ were similar in the two groups. Thus, non-attainment or non-maintenance of therapeutic CBZ level or other pharmacokinetic difference was not responsible for occurrence of seizures in the uncontrolled patients. A high percentage of patients with generalised tonic clonic seizures (73%) and simple partial seizures (SPS) with generalisation (66%) were controlled by CBZ, while SPS and complex partial seizures (CPS) were largely uncontrolled. INTERPRETATION & CONCLUSIONS: It appears that pharmacodynamic resistance of the seizure to CBZ rather than pharmacokinetic factors is responsible for lack of efficacy of CBZ in nonresponding epileptic patients.
Human herpesvirus-8 K8.1 gene encodes for two immunogenic class I glycoproteins, K8.1A and B, originating from spliced messages [(1998) Virology 243, 208-217]. The 228-amino-acid-long K8.1A open reading frame (ORF) contains four N-glycosylation sites and the 167-amino-acid-long K8.1B ORF contains three N-glycosylation sites, sharing similar amino- and carboxyl-termini with ORF K8.1A but with an in-frame deletion [(1998) Virology 249, 140-149]. To characterize the K8.1A and B glycoproteins in the infected body cavity-based B cell lymphoma (BCBL-1) cells and in the virion envelopes, monoclonal antibodies (MAbs) recognizing only K8.1A protein or both K8.1A and B proteins were generated. These antibodies reacted with the infected cell membranes and virion envelopes. Stable COS-1 transformant cells expressed the K8.1A and B proteins independently on the plasma membranes. MAbs recognized multiple proteins with molecular weights ranging from 23 to 72 kDa from the BCBL-1 cells and COS-1 cells and the 72 to 68 kDa molecular-weight proteins from the virion particles. The K8.1A is the predominant protein affinity purified from the infected BCBL-1 cells. Digestion with glycosidases show that these proteins contain both N- and O-linked sugars, suggesting that the multiple proteins recognized by the MAbs represent the precursor and product forms of K8.1A and B proteins, and the 72 to 68 kDa molecular-weight proteins represent the virion particle-associated mature forms of these glycoproteins.
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To understand the role of the ester moiety of the sn-1 acyl chain in phospholipase A2-glycerophospholipid interactions, we introduced an additional methylene residue between the glycerol C1 and C2 carbon atoms of phosphatidylcholines, and then studied the kinetics of hydrolysis and the binding of such butanetriol-containing phospholipids with Naja naja phospholipase A2. Hydrolysis was monitored by using phospholipids containing a NBD-labelled sn-2 acyl chain and binding was ascertained by measuring the protein tryptophan fluorescence. The hydrolysis of butanetriol-containing phospholipids was invariably slower than that of the glycerol-containing phospholipids. In addition, the enzyme binding with the substrate was markedly decreased upon replacing the glycerol residue with the 1,3,4-butanetriol moiety in phosphatidylcholines. These results have been interpreted to suggest that the sn-1 ester group in glycerophospholipids could play an important role in phospholipase A2-phospholipid interactions.
Fibromuscular dysplasia of the carotid artery is uncommon, but not rare. Although the true incidence and prevalence of the disease are not known, reported figures in adults range between 0.6% by angiography and 1.1% at autopsy. Most case reports of stroke caused by carotid fibromuscular dysplasia describe findings in adult subjects, although there are a few reports of the disease in children. In the present case, we describe a 16-year-old boy with fibromuscular dysplasia confined to one internal carotid artery and its branches, and in whom the disease declared itself by stroke. This case serves as a basis for considering diagnostic methods, treatment options, and future research in pediatric patients with cerebrovascular disease caused by fibromuscular dysplasia.
Antiphospholipid antibodies syndrome has emerged as an important entity responsible for stroke in young. Seven cases of young stroke (< 40 years of age) with mean age of 30.1 years (age range 25-39 years, 2 males and 5 females), who tested positive for antiphospholipid antibodies are being reported. All subjects had completed strokes. Six had arterial ischaemic and one patient had venous stroke. One patient suffered from four episodes, three ischaemic and one intracerebral haemorrhage. Two patients suffered from foetal loss. Generalised tonic clonic seizures occurred in three patients. Deep vein thrombosis was observed in one case. Thrombocytopenia was not observed in any case. All the patients had elevated anticardiolipin antibodies (aCL) IgM or IgG, while Lupus anticoagulant (LA) was elevated in 4 cases. Six cases belonged to primary antiphospholipid antibodies syndrome and one to lupus like illness. Oral anticoagulants were administered to maintain a high intensity international normalized ratio (INR). No recurrences were observed during a follow up period of 6-18 months.
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Fluorescent butanetriol-containing phospholipid analogs were synthesized by replacing the glycerol moiety in 1-hexadecanoyl-2-[6-N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) aminohexanoyl]-sn-glycero-3-phosphocholine, -phosphoethanolamine, -phosphoserine and 1-hexadecanoyl-2-[12-N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl)aminododecanoyl]-sn-glycero-3-phosphocholine, -phosphoethanolamine, -phosphoserine by the 1,3,4-butanetriol residue, and their out-to-in translocation in the human erythrocyte membrane studied by 'back exchanging' the outer surface-incorporated phospholipids using bovine serum albumin. The results of these studies indicate that the replacement of the glycerol moiety by the 1,3,4-butanetriol residue in aminophospholipids does not effect their out-to-in translocation in the human erythrocyte membrane. Furthermore, since earlier study by Arora and Gupta (Biochim. Biophys. Acta 1324 (1997) 47-60) has shown that the conformation of the 1,3,4-butanetriol phospholipids possess the backbone conformation similar to that of glycerophospholipids, it is suggested that besides the normal phospholipid polar head-group, a normal phospholipid interface conformation may also be required for the aminophospholipid-translocase interactions.
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A case of Guillain-Barré syndrome following meningococcal meningitis is reported. The diagnosis was made on clinical grounds and the results of electrophysiological studies. The patient recovered spontaneously. Guillain-Barré syndrome following meningococcal infection has not to our knowledge been reported previously.